Cellular prion protein acts as mediator of amyloid beta uptake by caveolin‐1 causing cellular dysfunctions in vitro and in vivo
PrP<sup>C</sup> expression adversely affects lifespan and behavior in 5xFAD mice. PrP<sup>C</sup> increases Aβ1-40 and Aβ1-42 levels and Aβ-plaque load in 5xFAD mice. Cav-1 interacts with both PrP<sup>C</sup> and Aβ peptides. Knocking out Cav-1 leads to a significant reduction in intracellular Aβ levels.
Authors
- Roberto Goya‐Maldonado (ORCID: https://orcid.org/0000-0002-7368-1332)
- Matthias Schmitz (ORCID: https://orcid.org/0000-0002-5502-681X)
- Inga Zerr (ORCID: https://orcid.org/0000-0002-6722-2463)
- Tiago F. Outeiro (ORCID: https://orcid.org/0000-0003-1679-1727)
- André Fischer (ORCID: https://orcid.org/0000-0001-8546-1161)
- Amandeep Singh Arora (ORCID: https://orcid.org/0000-0003-1045-1967)
- Franco L. Simonetti (ORCID: https://orcid.org/0000-0002-6472-9998)
- Gesine Saher (ORCID: https://orcid.org/0000-0003-3507-9604)
- Angela da Silva Correia (ORCID: https://orcid.org/0000-0003-1903-7172)
- Anna‐Lisa Fischer
- Susana da Silva Correia
Institutions
- German Center for Neurodegenerative Diseases (DE)
- Fundación Instituto Leloir (AR)
- Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 (DE)
- Brown Foundation (US)
- Max Planck Institute for Multidisciplinary Sciences (DE)
- Newcastle University (GB)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2024-08-30
- DOI
- https://doi.org/10.1002/alz.14120
- Citations
- 12
- Primary Topic
- Prion Diseases and Protein Misfolding
- Type
- article
- Field-Weighted Citation Impact
- 2.81
Funders
- Alzheimer Forschung Initiative